MCTR3 Reprogramming Monocytes for Joint Repair

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Solution Overview

Problem

Current treatments for rheumatoid arthritis primarily focus on reducing inflammation but fail to address joint repair and often lead to drug resistance over time, as they do not effectively reprogram monocytes to promote anti-inflammatory and tissue-protective functions.

Innovation Solution

The use of specialized pro-resolving mediators, specifically maresin conjugate in tissue regeneration 3 (MCTR3), which reprograms monocytes to confer enduring protective properties by activating epigenetic programs, leading to reduced joint inflammation and repair of bone and cartilage.

Engineering Contradictions & Design Principles

VSEngineering Contradiction Analysis

1Object-affected harmful factors

If conventional anti-inflammatory drugs are used to reduce joint inflammation, then inflammatory symptoms are improved, but joint repair and tissue protection are not addressed and drug resistance develops

Engineering Contradiction:

Improvejoint inflammationVSAvoidlong-term treatment effectiveness

Core Design Contradiction:

Object-affected harmful factorsVSReliability

Solution Approach 1:

Instead of using drugs that suppress inflammation through immunosuppression, the invention uses SPMs that actively promote resolution and tissue protection by reprogramming monocytes to adopt an anti-inflammatory phenotype, effectively inverting the approach from suppression to active resolution

Inventive Principle:

Principle #13The other way round (Inversion)

Solution Approach 2:

The invention changes the therapeutic parameter from immunosuppression to pro-resolution mediation, using SPMs that alter monocyte behavior through epigenetic reprogramming, thereby changing the fundamental mechanism of action to achieve both inflammation reduction and tissue protection

Inventive Principle:

Principle #35Parameter changes

2Object-affected harmful factors

If biological drugs targeting TNF and IL-6 are used to treat rheumatoid arthritis, then inflammatory propagation is reduced, but joint repair is not promoted and resistance develops over time

Engineering Contradiction:

Improveinflammatory propagationVSAvoidjoint damage

Core Design Contradiction:

Object-affected harmful factorsVSObject-generated harmful factors

Solution Approach 1:

The invention introduces SPMs as intermediary molecules that mediate the transition from pro-inflammatory to anti-inflammatory monocyte responses, acting as a bridge that promotes resolution without directly blocking inflammatory cytokines, thereby avoiding the side effects of cytokine inhibition

Inventive Principle:

Principle #24Intermediary (Mediator)

3Productivity

If monocytes are activated to promote disease propagation, then inflammatory response is enhanced, but anti-inflammatory and tissue-protective functions are suppressed

Engineering Contradiction:

Improveinflammatory responseVSAvoidtissue protection

Core Design Contradiction:

ProductivityVSObject-affected harmful factors

Solution Approach 1:

The invention applies SPMs in advance to reprogram monocytes before they can cause significant tissue damage, establishing an anti-inflammatory phenotype that prevents harmful inflammation rather than treating it after onset, thereby protecting tissues before damage occurs

Inventive Principle:

Principle #10Preliminary action

Data Source

PatentUS20240269170A1Treatment of Inflammatory Conditions or Diseases

Publication Date: 2024.08.15 QUEEN MARY UNIV OF LONDON

AI summary

The invention relates to agents and methods for treating or preventing inflammatory conditions or diseases.